妊娠糖尿病孕妇血浆抵抗素水平与胰岛素和血糖的分析

目的分析妊娠期糖尿病(GDM)孕妇血浆抵抗素水平与胰岛素和血糖的关系。方法采用酶联免疫吸附法(ELISA)检测53例妊娠期糖尿病GDM组孕妇和50例正常孕妇空腹血浆抵抗素水平;采用葡萄糖氧化酶法测定两组孕妇空腹血糖水平;采用发光免疫法测定两组孕妇的空腹血浆胰岛素水平。结果 GDM组孕妇空腹血浆抵抗素水平为(18.14±5.37)μg/L,正常妊娠组孕妇为(13.25±2.27)μg/L两组比较,差异有极显著性(t=5.96,P0.05);GDM组孕妇空腹血浆胰岛素、血糖水平分别为(12.64±4.35)mIU/L、(8.83±2.13)mmol/L,正常妊娠组孕妇分别为(10.21±4.22)mIU/L、(5.38±1.47)mmol/L,两组比较差异有极显著性(t=2.87和t=9.51,P0.05)。结论 GDM孕妇血浆抵抗素水平升高,其抵抗素水平与空腹血浆胰岛素及血糖水平有关。     

血清瘦素及胰岛素和血糖测定在妊娠期糖代谢中的临床意义

目的:探讨血清瘦素及胰岛素和血糖水平与妊娠期糖代谢异常孕妇的关系。方法:采用放射免疫分析测定36例妊娠期糖代谢异常孕妇(糖代谢异常组)和34例正常孕妇(正常妊娠组)的空腹及口服50g葡萄糖后3h的血清瘦素水平;采用电化学发光法测定两组孕妇的空腹血清胰岛素水平;采用葡萄糖氧化酶法测定两组孕妇的口服50g葡萄糖后1h的血糖水平。结果:1.糖代谢异常组孕妇血清瘦素水平为(14.9±4.3)μg/L,正常妊娠组为(9.8±1.7)μg/L,两组比较差异有显著性(P<0.01);2.糖代谢异常组孕妇空腹血清胰岛素、服糖后1h血糖水平分别为(12.9±4.3)mU/L、(11.0±1.4)mmol/L;正常妊娠组孕妇分别为(8.45±3.0)mU/L、(7.84±1.3)mmol/L。糖代谢异常组孕妇血清瘦素水平与空腹血清胰岛素、服糖后1h的血糖水平呈明显的正相关关系。相关系数(r)分别为0.835、0.758。结论:空腹血清瘦素水平升高见于妊娠期糖代谢异常孕妇,其瘦素水平的高低与空腹胰岛素及血糖水平相关。     

抵抗素蛋白在妊娠糖尿病孕妇与正常孕妇胎盘的表达

目的了解抵抗素蛋白在妊娠糖尿病孕妇与正常孕妇胎盘的表达情况,探讨抵抗素与妊娠生理性胰岛素抵抗(insu lin resistance,IR)及妊娠糖尿病(gestational d iabetes m ellitus,GDM)的关系。方法W estern b lot法检测妊娠糖尿病孕妇与正常孕妇胎盘抵抗素蛋白表达情况;葡萄糖氧化酶法测定血糖,测量收缩压(SBP)及舒张压(DBP)。结果W estern b lot结果以OD值表示,GDM孕妇胎盘抵抗素蛋白的表达(79305±7645.12)显著高于正常孕妇胎盘的表达(50718±3818.20)(P<0.01)。结论妊娠糖尿病孕妇胎盘抵抗素蛋白的表达显著高于正常孕妇胎盘的抵抗素蛋白的表达;表明胎盘可分泌抵抗素;抵抗素是引起妊娠生理性胰岛素抵抗和妊娠糖尿病的一个细胞因子。     

瘦素、脂联素、抵抗素、内肥素与妊娠糖尿病胰岛素抵抗的相关性研究

目的:探讨脂肪因子瘦素、脂联素、抵抗素、内肥素与妊娠糖尿病(GDM)胰岛素抵抗的相关性.方法:实验分为正常育龄妇女组(44例)、正常妊娠妇女组(62例)和妊娠糖尿病患者组(63例),用ELISA方法分别检测3组瘦素(Leptin),脂联素(Adiponectin),抵抗素(Resistin),内肥素(Visfatin)的水平,用葡萄糖氧化酶法检测血糖水平,免疫发光法检测胰岛素水平,用HOMA-IR(稳态模型胰岛素抵抗指数)表示胰岛素抵抗状态,HOMA-IR=空腹血糖×空腹血胰岛素÷22.5,用SPSSll.5统计软件进行统计分析.结果:妊娠糖尿病患者组的瘦素水平明显高于正常妊娠妇女组[(13.50±7.14)ng/ml、(7.78±3.82)ng/ml,P<0.001],正常妊娠妇女组明显高于正常育龄妇女组[(7.78±3.82)ng/ml、(1.73±0.70)ng/ml,P<0.001]差异具有统计学意义;GDM 组的内肥素水平明显低于正常妊娠妇女组[(15.67±5.78)ng/ml、(22.43±5.68)ng/ml,P<0.001],正常妊娠妇女组明显低于正常育龄妇女组[(22.43±5.68)ng/ml、(36.46±13.34)ng/ml,P<0.001],差异具有统计学意义;GDM 组的脂联素水平低于正常妊娠妇女组[(5 491.71±2 986.00)ns/ml、(6 692.34±2 583.51)ng/ml,P=O.029],差异有统计学意义,正常妊娠妇女组明显低于正常育龄妇女组[(6 692.34±2 583.51)ng/ml、(11 076.82±3 694.75)ng/ml,P<0.1301],差异具有统计学意义;GDM组抵抗素水平与正常妊娠妇女组比较差异没有统计学意义.在妊娠糖尿病患者组,HOMA-IR与瘦素(r=0.352,P=0.005)正相关,与内肥素(,=-0.255,P=0.046)呈负相关.结论:妊娠糖尿病患者瘦素水平升高,内肥素和脂联素水平降低,瘦素和内肥素与胰岛素抵抗有关,瘦素和内肥素参与了妊娠糖尿病胰岛素抵抗的发生发展;脂联素和抵抗素与胰岛素抵抗不具有相关性,脂联素和抵抗素可能与妊娠糖尿病胰岛素抵抗的发生无关.     

内脂素、抵抗素在妊娠期糖尿病发病中的作用

目的探讨新近发现的两种脂肪细胞因子——内脂素和抵抗素,与胰岛素抵抗的关系及其在妊娠期糖尿病(GDM)发病中的作用。方法采用病例对照的研究方法,通过检测40例GDM孕妇和40例正常孕妇的血清内脂素(Visfa-tin)、抵抗素(Resistin)空腹血糖(FPG)和空腹胰岛素(FINS)水平,计算HOMA稳态模型胰岛素抵抗指数(IRI),比较两组胰岛素抵抗程度的差异,并进一步分析内脂素、抵抗素与胰岛素抵抗之间的关系及其在GDM发生过程中所起的作用。结果 (1)GDM组的血清内脂素、抵抗素、空腹血糖(FPG)、空腹胰岛素(FINS)和胰岛素抵抗指数(IRI)均明显高于对照组(P<0.01)。(2)相关分析表明:GDM孕妇的血清内脂素、抵抗素均与胰岛素抵抗指数(IRI)呈显著正相关(r=0.568,0.618,P=0.000),而内脂素与抵抗素之间亦呈密切正相关(r=0.919,P=0.000)。结论 (1)GDM孕妇的血清内脂素、抵抗素水平较正常孕妇明显增高。(2)内脂素、抵抗素均与胰岛素抵抗呈正相关。(3)血清内脂素、抵抗素水平增高以及二者对胰岛素敏感性调节所产生的综合效应是诱导妊娠期糖尿病发生或促进其发展的重要因素。     

妊娠期糖尿病患者血清Nesfatin-1水平及糖脂代谢紊乱的相关性

目的探讨妊娠期糖尿病(GDM)患者血清中Nesfatin-1水平及糖脂代谢紊乱的相关性。方法 2013年1月至2014年1月妊娠中期(24-28w)诊断GDM的68例孕妇为GDM组,选取同期正常妊娠中期孕妇136例作为对照组。采用使用酶联免疫吸附法(ELISA)检测血清Nesfatin-1水平,检测总胆固醇(TC)、甘油三脂(TG)、载脂蛋白A(apo A)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、载脂蛋白A(apo A)、空腹血糖(FPG)、餐后1h血糖(1h PG)、餐后2h血糖(2h PG)、空腹胰岛素(FINS)水平,计算胰岛素抵抗指数(HOMA-IR),比较两组的差异、分析血清Nesfatin-1与胰岛素抵抗相关性。结果 GDM组血清Nesfatin-1(0.98±0.54)(μg/L)、HDL-C(1.25±0.47)(mmol/L)明显低于对照组(1.54±0.38,P0.01;1.36±0.29,P0.05)。GDM组血清TG(2.91±0.93)(mmol/L)、LDL-C(2.93±0.76)(mmol/L)、apo A(1.54±0.21)(g/L)、FPG(5.32±0.62)(mmol/L)、2h PG(8.67±1.04)(mmol/L)、FINS(16.98±1.04)(m U/L)和HOMA-IR(4.52±0.64)均明显高于对照组[TG(2.59±0.61,P0.05)(mmol/L)、LDL-C(2.68±0.59,P0.01)(mmol/L)、apo A(0.86±0.37,P0.01)(g/L)、FPG(4.35±0.41,P0.01)(mmol/L)、2h PG(6.29±0.88,P0.01)(mmol/L)、FINS(13.11±2.36,P0.01)(m U/L)和HOMA-IR(2.47±0.28,P0.01)]。相关性分析显示,GDM孕妇血清Nesfatin-1与TG、LDL、HDL、FPG、2h PG、FINS及HOMA-IR呈负相关(r=-0.557,P0.01;r=-0.57,P0.01;r=-0.63,P0.01;r=-0.60,P0.01;r=-0.71,P0.01;r=-0.71,P0.01;r=-0.68,P0.01)。结论 GDM孕妇血清Nesfatin-1水平降低;Nesfatin-1降低与GDM糖脂代谢紊乱密切相关。     

妊娠期糖尿病患者血清脂联素与TNF-α浓度的关系

目的探讨妊娠期糖尿病(GDM)患者血清脂联素与肿瘤坏死因子α(TNF-α)浓度及其临床意义。方法用放射免疫法测定50例GDM孕妇和36例正常孕妇(NGT)的血清脂联素浓度,ELISA法检测血清TNF-α浓度,电化学发光法测胰岛素浓度,葡萄糖氧化酶法测血糖浓度。结果①GDM孕妇血清TNF-α(4.6±1.5)μg/L水平明显高于NGT(3.3±1.6)μg/L,且GDM组TNF-α与血糖、胰岛素浓度呈正相关关系(P<0.01)。②GDM孕妇血清脂联素浓度(10.3±2.4)mg/L明显低于NGT孕妇(15.6±3.2)mg/L,GDM组脂联素浓度与血糖、胰岛素浓度呈负相关关系(P<0.01)。结论GDM患者血清低脂联素浓度与高TNF-α浓度不仅反映了母体体脂状况和胰岛素的抵抗状态,更反映了糖代谢受损的严重程度,是代谢综合征的重要预测因子。     

初诊2型糖尿病患者短期胰岛素强化治疗后胰岛β细胞功能的变化和疗效观察

观察胰岛素短期强化治疗对明显高血糖的初诊2型糖尿病(2DM)患者的胰岛β细胞功能的影响. 对空腹血糖＞12.0mmol/L的24例初诊DM患者进行胰岛素强化治疗,分析比较治疗前后和两次随访的空腹血糖、糖化血红蛋白(HbA1c)、口服75g葡萄糖后的胰岛素及释放曲线面积和由HOMA模型计算的HOMA IR 和HOMAβ.血浆胰岛素用放射免疫分析法测定.平均9.0±4.8天的胰岛素强化治疗后,患者的血糖、HbA1c较治疗前明显降低(P＜0.01);胰岛素、胰岛素释放曲线下面积和HOMAβ较治疗前明显提高(P＜0.01),而HOMA IR明显降低(P＜0.01).其中随访的13例患者中,6个月和12个月后随访平均空腹血糖分别为6.28±0.75mmol/L和6.62±1.19mmol/L;餐后2h血糖分别为8.72±1.66mmol/L和10.03±4.49mmol/L;HbA1c分别为5.98%±0.72%和7.12%±1.81%;空腹胰岛素分别为10.67±5.08μIU/L和7.85±1.82μIU/L;HOMA IR分别为2.88±1.22和2.36±0.93;HOMAβ分别为90.01±61.29和56.9±25.4.仅采用饮食控制和体育锻炼,其中8例(8/13)获得长达一年的良好的血糖控制.明显高血糖的2DM患者,短期胰岛素强化治疗具有快速控制血糖和显著改善胰岛β细胞功能的作用.     

妊娠期糖尿病患者血清孤独G蛋白偶联受体配体和视黄酸受体反应蛋白2水平及其与胰岛素抵抗的关系

目的探讨妊娠期糖尿病(GDM)患者血清孤独G蛋白偶联受体(apelin)和视黄酸受体反应蛋白2(chemerin)水平及其与胰岛素抵抗的关系。方法选择2009年3月至2011年12月于泰安市中心医院门诊做产前检查的孕妇70名,其中糖耐量正常组(NGT)孕妇30名,妊娠期糖尿病组(GDM)孕妇40名。计算每个个体体重指数(BMI),以及胰岛素抵抗指数(HOMA-IR),测定空腹以及糖负荷后2h血清apelin、chemerin水平,空腹血清胰岛素(FINS)以及糖负荷2h后血清胰岛素(2h PINS)。结果 GDM组与NGT组相比较,体重指数差异有统计学意义(28.92±2.25kg/m2vs 23.83±1.46 kg/m2,P<0.05),并且空腹胰岛素[(19.08土3.65μIU/L vs 14.16±2.42μIU/L),P<0.05]、糖负荷2h后胰岛素[(45.14±30.56μIU/L vs36.52±21.23μIU/L),P<0.05]以及胰岛素抵抗指数差异也有统计学意义(3.98±0.76,2.85±0.48,P<0.05);与NGT组比较,GDM组空腹(468.34±31.25 pg/mL vs 392.74±17.35pg/mL)以及糖负荷2h后(575.61±40.48 pg/mL vs 452.64±21.91 pg/mL)血清apelin差异有统计学意义(均P<0.05),与NGT组比较,GDM组空腹(72.26±16.63μg/L vs 60.81±17.27μg/L)以及糖负荷2h后(75.87±22.14μg/L vs 65.86±20.22μg/L)血清chemerin差异有统计学意义(均P<0.05)。同时发现apelin与chemerin水平呈正相关(r=0.45,P<0.05),血清apelin、chemerin与BMI呈正相关(r=0.47,P<0.05;r=0.68,P<0.01),与FINS呈正相关(r=0.36,P<0.05,r=0.26,P<0.05),与2h PINS呈正相关(r=0.28,P>0.05;r=0.22,P<0.05),与HOMA-IR呈正相关(r=0.45,P<0.05;r=0.49,P<0.05)。结论妊娠期糖尿病患者血清apelin、chemerin水平与胰岛素抵抗密切相关,apelin、chemerin可能参与了妊娠期糖尿病患者代谢的改变。     

艾塞那肽联合甘精胰岛素对肥胖2型糖尿病效果观察

目的：对艾塞那肽联合甘精胰岛素在2型糖尿病患者中的治疗效果进行观察。方法选取我院2012年4月~2014年4月68例2型肥胖糖尿病患者,将所有患者分成两组,每组34例,1组作为对照组进行胰岛素治疗,2组作为实验组进行艾塞那肽联合甘精胰岛素治疗。治疗后对两组患者的空腹血糖、餐后2h血糖、血脂等情况进行比较。结果实验组平均空腹血糖为(5.83±0.71)mmol/L,餐后2h血糖为(7.32±1.05)mmol/L,糖化血红蛋白水平为(6.15±0.72)%;对照组患者空腹血糖水平为(11.26±1.34)mmol/L,餐后2h血糖为(14.31±2.06)mmol/L,糖化血红蛋白水平(9.93±1.51)%,P<0.05。两组患者胆固醇、甘油三酯、低密度脂蛋白水平存在明显差异,但高密度脂蛋白水平差异不大。结论：艾塞那肽联合甘精胰岛素在2型糖尿病患者中的治疗效果较为显著,能够有效的对患者血糖进行控制,降低患者发病率。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.